Physiology of the Vestibular System

Physiology of the Vestibular System
Within the inner ear are specialized sensory receptors
responsible for the perception of the forces associated
with head movement and gravity. Control centers
within the brainstem integrate this information along
with other biologic signals derived from vision and
proprioceptive sensors in the final determination of an
individual’s orientation in three-dimensional space.1
Although anatomically developed and responsive at
birth, the vestibular system matures along with other
senses in the first 7 to 10 years of life.2
Recognition of the head’s movement relative to the
body is provided by the linear (otolithic macula) and
angular (semicircular canals) acceleration receptors of
the inner ear. Electrical activity generated within the
inner ear travels along the vestibular nerve (primary
afferent neuronal pathway) to the central vestibular
nuclei of the brainstem, forming second-order neuronal
pathways that become the vestibulo-ocular reflex
(VOR), the vestibulospinal tracts, and the vestibulocerebellar
tracts. Pathways derived from vestibular
information also travel to the brainstem emetic centers,
which serves to explain vegetative symptoms such as
nausea, vomiting, and perspiration that a patient typically
experiences following an acute unilateral vestibular
loss (Figure 2-1).
Disruption of peripheral (inner ear and the vestibular
nerve) or central vestibular pathways as a result of, for
example , trauma, ototoxicity, or surgical deafferentation
leads to the patient experiencing a distortion in orientation.
The patient often uses the term“dizziness,” which
is an all-encompassing yet relatively nonspecific term
that can include symptoms such as giddiness, lightheadedness,
and floating sensation. Clinically, the term
“vertigo” is best suited to describe a precise type of
dizziness—a hallucination of movement involving oneself
(subjective vertigo) or the surrounding environment
(objective vertigo) that is apt to occur when there is an
acute interruption of vestibular pathways.1

Within the inner ear are specialized sensory receptorsresponsible for the perception of the forces associatedwith head movement and gravity. Control centerswithin the brainstem integrate this information alongwith other biologic signals derived from vision andproprioceptive sensors in the final determination of anindividual’s orientation in three-dimensional space.1Although anatomically developed and responsive atbirth, the vestibular system matures along with othersenses in the first 7 to 10 years of life.2Recognition of the head’s movement relative to thebody is provided by the linear (otolithic macula) andangular (semicircular canals) acceleration receptors ofthe inner ear. Electrical activity generated within theinner ear travels along the vestibular nerve (primaryafferent neuronal pathway) to the central vestibularnuclei of the brainstem, forming second-order neuronalpathways that become the vestibulo-ocular reflex(VOR), the vestibulospinal tracts, and the vestibulocerebellartracts. Pathways derived from vestibularinformation also travel to the brainstem emetic centers,which serves to explain vegetative symptoms such asnausea, vomiting, and perspiration that a patient typicallyexperiences following an acute unilateral vestibularloss (Figure 2-1).Disruption of peripheral (inner ear and the vestibularnerve) or central vestibular pathways as a result of, forexample , trauma, ototoxicity, or surgical deafferentationleads to the patient experiencing a distortion in orientation.The patient often uses the term“dizziness,” whichis an all-encompassing yet relatively nonspecific termthat can include symptoms such as giddiness, lightheadedness,and floating sensation. Clinically, the term“vertigo” is best suited to describe a precise type ofdizziness—a hallucination of movement involving oneself(subjective vertigo) or the surrounding environment(objective vertigo) that is apt to occur when there is anacute interruption of vestibular pathways.1 Of all the human vestibular pathways, the VOR remains the most important and most studied. At its simplest level the VOR is required to maintain a stable retinal image with active head movement. When an active head movement is not accompanied by an equal but opposite conjugate movement of the eyes, retinal slip occurs. When the VOR is affected bilaterally (as could occur from systemic aminoglycoside poisoning) patients characteristically complain of visual blurring with head movement, better known as oscillopsia, in addition to having significant complaints of imbalance and ataxia.3 True vertigo is typically not a feature of a bilateral peripheral vestibular loss. Figure 2-1 Schematic representation of the vestibular system and its pathways. Figure 2-2 Anatomic organization of the peripheral vestibular system (vestibular end-organs and the vestibular nerve). ANATOMY OF THE VESTIBULAR SYSTEM Peripheral Vestibular System The peripheral vestibular system includes the paired vestibular sensory end-organs of the semicircular canals (SCCs) and the otolithic organs. These receptors are found within the fluid-filled bony channels of the otic capsule (the dense endochondral-derived bone that surrounds the labyrinth and cochlea) and are responsible for perception of both the sense of position and motion. The vestibular nerve (both superior and inferior divisions of the VIIIth nerve) is the afferent connection to the brainstem nuclei for the peripheral vestibular system (Figure 2-2). Perception of angular accelerations is chiefly the responsibility of the three paired SCCs (superior, posterior, and lateral). Within the ampullated portion of the membranous labyrinth are the end-organs of the cristae, containing specialized hair cells that transduce mechanical shearing forces into neural impulses. Histologically the hair cells of the ampulla are located on its surface. Their cilia extend into a gelatinous matrix better known as the cupula, which acts like a hinged gate between the vestibule and the canal itself (Figure 2-3). The otolithic organs of the utricle and the saccule are found within the vestibule. Chiefly responsible for the perception of linear accelerations (eg, gravity, deceleration in a car), their end-organs consist of a flattened, hair cell–rich macular area whose cilia project into a similar gelatinous matrix. The matrix, however, differs from the matrix associated with the SCCs in its support of a blanket of calcium carbonate crystals better known as otoliths, which have a mean thickness of approximately 50 μm (Figure 2-4).4 Information from the vestibular end-organs is transmitted along the superior (which receives information from the superior, horizontal SCCs and utricle) and inferior (which receives information from the posterior SCC and saccule) divisions of the vestibular nerve. Although its role is primarily afferent in the transmission of electrical activity to the central vestibular nuclei of the brainstem, an efferent system does exist that probably serves to modify end-organ activity. 5 Each vestibular nerve consists of approximately 25,000 bipolar neurons whose cell bodies are located in a structure known as Scarpa’s ganglion, which is typically found within the internal auditory canal (IAC).6 Type I neurons of the vestibular nerve derive information from corresponding type 1 hair cells, whereas type II neurons derive information from corresponding type 2 hair cells at its simplest.

Figure 2-3 Stylized representation of the crista: angular acceleration receptor.

Figure 2-4 Stylized representation of macular end-organ: linear acceleration receptor.

Central Vestibular System

Primary vestibular afferents enter the brainstem dividing

into ascending and descending branches. Within

the brainstem there appears to exist a nuclear region

with four distinct anatomic types of second-order

neurons that have been traditionally considered to constitute

the vestibular nuclei. It appears, however, that

not all these neurons receive input from the peripheral

vestibular system.4,7 The main nuclei are generally

recognized as the superior (Bechterew’s nucleus),

lateral (Deiters’ nucleus), medial (Schwalbe’s nucleus ),

and descending (spinal vestibular nucleus).

Functionally, in primate models, the superior

vestibular nucleus appears to be a major relay station

for conjugate ocular reflexes mediated by the SCCs.

The lateral vestibular nucleus appears to be important

for control of ipsilateral vestibulospinal (the so-called

“righting”) reflexes. The medial vestibular nucleus,

because of its other connections with the medial longitudinal

fasciculus, appears to be responsible for coordinating

eye, head, and neck movements. The descending

vestibular nucleus appears to have an integrative function

with respect to signals from both vestibular nuclei,

the cerebellum, and an amorphous area in the reticular

formation postulated to be a region of neural integration.

Commonly referred to as the “neural integrator”

among neurophysiologists, it is responsible for the

ultimate velocity and position command for the final

common pathway for conjugate versional eye movements

and position.8

The vestibular nerve in part also projects directly

to the phylogenetically oldest parts of the cerebellum—

namely, the flocculus, nodulus, ventral uvula, and the

ventral paraflocculus—on its way directly through the

vestibular nucleus. Better known as the vestibulocerebellum,

this area also receives input from other

neuronal pathways in the central nervous system (CNS)

responsible for conjugate eye movements, especially

smooth-pursuit eye movements, which, in addition to

the VOR, are responsible for holding the image of a

moving target within a certain velocity range on the

fovea of the retina. The Purkinje’s cells of the flocculus

are the main recipients of this information, of which

some appears to be directed back toward the ipsilateral

vestibular nucleus for the purposes of modulating eye

movements in relation to gaze (eye in space) velocity

with the head still or during combined eye–head

(vestibular signal-derived) tracking.9,10 Important for

cancelling the effects of the VOR on eye movement

when it is not in the best interest of the individual

(think of twirling ballet dancers or figure skaters and

how they can spin without getting dizzy), the vestibulocerebellum

is also important in the compensation

process for a unilateral vestibular loss.

The Hair Cells

The fundamental unit for vestibular activity on a

microscopic basis inside the inner ear consists of

broadly classified type 1 and 2 hair cells (Figure 2-5).

Type 1 hair cells are flask-shaped and surrounded

by the afferent nerve terminal at its base in a chalicelike

fashion. One unique characteristic of the afferent

nerve fibers that envelop type 1 hair cells is that they are

among the largest in the nervous system (up to 20 μm

in diameter). The high amount of both tonic (spontaneous)

and dynamic (kinetic) electrical activity at any

time arising from type 1 hair cells has probably necessitated

this feature for the neurons that transfer this

information to the CNS. Type 2 hair cells are more

cylindrical and at their base are typically surrounded by

multiple nerve terminals in contradistinction.

Each hair cell contains on its top a bundle of 50 to

100 stereocilia and one long kinocilium that project

into the gelatinous matrix of the cupula or macula. It

is thought that the location of the kinocilium relative

to the stereocilia gives each hair cell an intrinsic polarity

that can be influenced by angular or linear accelerations.

It is important to realize that an individual is

born with a maximum number of type 1 and 2 hair

cells that cannot be replaced or regenerated if lost as a

result of the effects of pathology (eg, ototoxicity or surgical

trauma) or aging (the postulated presbyvestibular

dropout from cellular apoptosis). Presumably the same

process holds for the type I and II neurons that comprise

the vestibular nerve.


At the microscopic level, movements of the head or changes in linear accelerations deflect the cupula or shift the gelatinous matrix of the otolithic organs with its load of otolithic crystals that will either stimulate (depolarize) or inhibit (hyperpolarize) electrical activity from type 1 and 2 hair cells. Displacement of the stereocilia either toward or away from the kinocilium influences calcium influx mechanisms at the apex of the cell that causes either the release or reduction of neurotransmitters from the cell to the surrounding afferent neurons (Figures 2-6 and 2-7 ).12 The electrical activity generated is then transferred along the vestibular nerve to the vestibular nuclei in the brainstem.

Information above the tonic (spontaneous) firing rate of the type 1 hair cells transmitted along type I neurons is largely thought to have a stimulatory effect in contrast to a more inhibitory effect attributable to type 2 hair cells and type II neurons. The SCCs largely appear to be responsible for the equal but opposite corresponding eye-to-head movements better known as the VOR. The otolithic organs are primarily responsible for ocular counter-rolling with tilts of the head and for vestibulospinal reflexes that help in the maintenance of body posture and muscle tone.

In order to ultimately produce conjugate versional VOR-mediated movements of the eyes, each vestibular nucleus receives electrical information from both sides that is exchanged via the vestibular commissure in the brainstem. The organization is generally believed to be specific across the commissure. Neurons in the right vestibular nucleus, for example, that receive type I input from the right horizontal SCC project across the commissure to the neurons found in the left vestibular nucleus that are driven by the left horizontal SCC receiving contralateral type II input and vice versa.


According to Leigh and Zee’s seminal text, the key concepts of vestibular physiology can be best appreciated in the context that “the push–pull pairings of the canals, the resting vestibular tone and exchange of neural input through the vestibular commissure maximize vestibular sensitivity in health and provide a substrate for compensation and  adaptation.”7

VOR Gain

In order to maintain a stable retinal image during head movement, the eyes should move in an equal but opposite direction to head movement. Anything less than unity (corresponding eye movement/head movement) may result in the perception of visual blurring with head movement—oscillopsia being the classic symptomatic complaint of an individual with a bilateral peripheral vestibular loss as might result from gentamicin vestibulotoxicity.


Defined as a rhythmic to-and-fro, back-and-forth movement of the eyes, nystagmus represents the cardinal sign of unilateral peripheral vestibular or central vestibular dysfunction. In an acute unilateral loss of peripheral vestibular activity that might occur from topical aminoglycoside drops or certain disinfectant surgical preparation solutions used in the presence of a tympanic membrane defect, injury to the end-organ causes a difference in neural activity between the left and right vestibular nuclei. Should the push–pull pairings of the canals be affected as a result of pathology, the eyes are typically driven with a slow movement toward the affected side only to be corrected by a fast corrective saccade generated within the CNS away from the side of the lesion in a repetitive fashion. Although somewhat misguided, the direction of the nystagmus by convention refers to the fast phase, typically away from the side of the lesion under circumstances of an acute unilateral peripheral vestibular loss.

Habituation and Adaptation

In humans the CNS may habituate (show a reduced response) the VOR depending on the environmental circumstances. This may happen in individuals who are blind or in those exposed to constant velocity rotations or continuous low-frequency oscillations (such as on a ship). The mechanisms for adaptation or the adaptive plasticity of the VOR are usually visually driven and have been experimentally studied by subjects wearing reversing prisms.13 This phenomenon is frequently experienced by those wearing new prescriptive glasses with the explanation that “they take some time to get used to.” Eventually one adapts to the new lenses as the gain of the VOR changes accordingly. The same holds true to some extent for those with a unilateral peripheral vestibular loss, where the gain can be somewhat influenced, though not perfectly.


Clinical improvement following acute unilateral peripheral vestibular deafferentation requires the presence of intact central vestibular connections primarily at the level of the vestibulocerebellum.4,7 The loss of tonic or spontaneous vestibular activity from the endorgan is ultimately replaced by the development of spontaneous electrical activity arising within the vestibular nuclei of the affected side.14 At rest the asymmetries that would be expected from the push–pull effects from the canals are kept in check, and as a result there is the gradual resolution of the once-present spontaneous nystagmus. Quick head movements producing changes in the dynamic electrical activity, however, can never be completely compensated through this mechanism on the affected side, and a bilateral loss of inner ear function never does despite the insertion of midrotation corrective saccades. For a more detailed explanation of the phenomenon of compensation and why it often fails in the setting of a bilateral vestibular loss.



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